Schematics illustrate a putative pathway of mitotic PCM assembly in a WT cell (A), or in cells lacking either Cnn (B), DSpd-2 (C), or both Cnn and DSpd-2 (D). A top view of the mother centriole is shown surrounded by a layer of Asl (grey); solid arrows represent recruiting interactions, dotted arrows represent maintaining interactions. Arrow thickness reflects the relative strength of the recruitment or maintenance, and the size of the text reflects the amount of protein localized at centrosomes. In WT cells (A), Asl has an important role in recruiting DSpd-2 to centrosomes, which in turn has an important role in recruiting Cnn; Cnn then has an important role in maintaining DSpd-2 at centrosomes. Thus, a positive feedback loop is generated where increasing amounts of DSpd-2 can recruit increasing amounts of Cnn, which can then maintain increasing amounts of DSpd-2. DSpd-2 and Cnn both independently recruit other PCM components (red), which themselves help support the PCM structure and can recruit further PCM components. In the absence of Cnn (B), Asl can still recruit DSpd-2 normally, but DSpd-2 cannot efficiently accumulate around the centrioles. The reduced levels of DSpd-2 recruit reduced levels of PCM. In the absence of DSpd-2 (C), an alternative pathway recruits reduced levels of Cnn. This pathway most likely involves Asl (as indicated here), as inhibiting Asl reduces the rate of Cnn incorporation into the PCM (Conduit et al., 2010) and Asl and Cnn appear to weakly interact in a Y2H analysis (Figure 6); other pathways, however, could also be involved. The reduced levels of Cnn recruit reduced levels of PCM. In the absence of Cnn and DSpd-2 (D), no mitotic PCM can be assembled.